Postmenopausal osteoporosis (PMOP) is a bone metabolic disorder primarily triggered by estrogen deficiency, characterized by reduced bone mass, deterioration of bone microarchitecture, and an increased risk of fractures. Although conventional therapeutic strategies can partially alleviate bone resorption, they often exert adverse side effects and struggle to rectify the underlying imbalance in bone metabolism. Recent advancements in bone immunology have revealed the intricate interplay between immune responses and skeletal dynamics during the progression of PMOP. Elevated levels of pro-inflammatory cytokines have been implicated in the excessive activation of osteoclasts and the inhibition of osteoblastic differentiation, thereby perpetuating a vicious cycle. In this context, exosomes have garnered attention as a novel therapeutic approach for PMOP due to their exceptional capacity for delivering bioactive components, immunomodulatory properties, and low toxicity. Exosomes are nanoscale vesicles secreted by cells that naturally encapsulate proteins, nucleic acids, and epigenetic factors, enabling them to traverse biological barriers and selectively modulate the functions of target cells. In the treatment of PMOP, exosomes exhibit significant regulatory potential through various mechanisms, including the restoration of ovarian function, remodeling of the gut microbiome, modulation of the immune system, and direct regulation of osteoblastic/osteoclastic differentiation. Furthermore, their low immunogenicity and high biocompatibility confer innovative advantages for clinical applications in PMOP therapy. This review elucidates the mechanisms of action, regulatory networks, and clinical translational potential of exosomes derived from different sources in the treatment of PMOP, aiming to provide theoretical support for exosome-based precision intervention strategies and to pave new pathways for the early diagnosis and efficacy monitoring of PMOP.
Huang et al. (Thu,) studied this question.